Involvement of Mcl1 in diallyl disulfide-induced G2/M cell cycle arrest in HL-60 cells
Diallyl disulfide (DADS) has shown potential as a therapeutic agent in various cancers. Previously, we found that myeloid cell leukemia sequence 1 (Mcl1) was downregulated in DADS-induced cell cycle arrest in HL-60 human leukemia cells. Here, we investigated the role of this protein in DADS-induced...
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| Veröffentlicht in: | Oncology reports 2012-06, Vol.27 (6), p.1911-1917 |
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| container_end_page | 1917 |
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| container_issue | 6 |
| container_start_page | 1911 |
| container_title | Oncology reports |
| container_volume | 27 |
| creator | LAN YI JI, Xiao-Xia HUI TAN FENG, Mei-Yan YI TANG LING WEN QI SU |
| description | Diallyl disulfide (DADS) has shown potential as a therapeutic agent in various cancers. Previously, we found that myeloid cell leukemia sequence 1 (Mcl1) was downregulated in DADS-induced cell cycle arrest in HL-60 human leukemia cells. Here, we investigated the role of this protein in DADS-induced G2/M cell cycle arrest in HL-60 cells. We demonstrated that DADS treatment significantly increased the proportion of G2/M phase HL-60 cells (P |
| doi_str_mv | 10.3892/or.2012.1704 |
| format | Article |
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Previously, we found that myeloid cell leukemia sequence 1 (Mcl1) was downregulated in DADS-induced cell cycle arrest in HL-60 human leukemia cells. Here, we investigated the role of this protein in DADS-induced G2/M cell cycle arrest in HL-60 cells. We demonstrated that DADS treatment significantly increased the proportion of G2/M phase HL-60 cells (P<0.05) and caused a time-dependent significant downregulation of Mcl1 and the cell cycle-related proteins PCNA and CDK1 (P<0.05). Small interfering RNA-mediated knockdown of Mcl1 expression in HL-60 cells arrested the cell cycle in G2/M phase. By co-immunoprecipitation, we demonstrated that Mcl1 associated with PCNA and CDK1 in G2/M cell cycle arrest in DADS-treated HL-60 cells. DADS decreased the interaction of Mcl1 with PCNA and CDK1, leading to G2/M cell cycle arrest in HL-60 cells. Mcl1 plays an important role in DADS-induced G2/M cell cycle arrest in HL-60 human leukemia cells.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2012.1704</identifier><identifier>PMID: 22378300</identifier><language>eng</language><publisher>Athens: Spandidos</publisher><subject>Allyl Compounds - pharmacology ; Antineoplastic Agents - pharmacology ; Biological and medical sciences ; CDC2 Protein Kinase - metabolism ; Cell Cycle Proteins - metabolism ; Cell Line, Tumor ; Cell Proliferation ; Disulfides - pharmacology ; G2 Phase Cell Cycle Checkpoints - drug effects ; HL-60 Cells ; Humans ; Medical sciences ; Myeloid Cell Leukemia Sequence 1 Protein ; Proliferating Cell Nuclear Antigen - metabolism ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; RNA Interference ; RNA, Small Interfering ; Tumors</subject><ispartof>Oncology reports, 2012-06, Vol.27 (6), p.1911-1917</ispartof><rights>2015 INIST-CNRS</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c358t-1dff3a7939ff20573b4ad8a35e64bcd1754b10bc9c70518db3ad16391e09da033</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25835720$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22378300$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LAN YI</creatorcontrib><creatorcontrib>JI, Xiao-Xia</creatorcontrib><creatorcontrib>HUI TAN</creatorcontrib><creatorcontrib>FENG, Mei-Yan</creatorcontrib><creatorcontrib>YI TANG</creatorcontrib><creatorcontrib>LING WEN</creatorcontrib><creatorcontrib>QI SU</creatorcontrib><title>Involvement of Mcl1 in diallyl disulfide-induced G2/M cell cycle arrest in HL-60 cells</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Diallyl disulfide (DADS) has shown potential as a therapeutic agent in various cancers. Previously, we found that myeloid cell leukemia sequence 1 (Mcl1) was downregulated in DADS-induced cell cycle arrest in HL-60 human leukemia cells. Here, we investigated the role of this protein in DADS-induced G2/M cell cycle arrest in HL-60 cells. We demonstrated that DADS treatment significantly increased the proportion of G2/M phase HL-60 cells (P<0.05) and caused a time-dependent significant downregulation of Mcl1 and the cell cycle-related proteins PCNA and CDK1 (P<0.05). Small interfering RNA-mediated knockdown of Mcl1 expression in HL-60 cells arrested the cell cycle in G2/M phase. By co-immunoprecipitation, we demonstrated that Mcl1 associated with PCNA and CDK1 in G2/M cell cycle arrest in DADS-treated HL-60 cells. DADS decreased the interaction of Mcl1 with PCNA and CDK1, leading to G2/M cell cycle arrest in HL-60 cells. Mcl1 plays an important role in DADS-induced G2/M cell cycle arrest in HL-60 human leukemia cells.</description><subject>Allyl Compounds - pharmacology</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>CDC2 Protein Kinase - metabolism</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Disulfides - pharmacology</subject><subject>G2 Phase Cell Cycle Checkpoints - drug effects</subject><subject>HL-60 Cells</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Myeloid Cell Leukemia Sequence 1 Protein</subject><subject>Proliferating Cell Nuclear Antigen - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering</subject><subject>Tumors</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1Lw0AQhhdRrFZvniUX8WLa2Z0kmz1K0bbQ4kXFW9jsB0Q2Sd1tCv33Jrbq6R2YZ16Gh5AbChPMBZu2fsKAsgnlkJyQC8oFjVmC9LSfgdEYMf0YkcsQPgEYh0yckxFjyHMEuCDvy2bXup2pTbONWhutlaNR1US6ks7tXZ-hc7bSJq4a3SmjozmbriNlnIvUXjkTSe9N2A43i1Wcwc8qXJEzK10w18cck7fnp9fZIl69zJezx1WsMM23MdXWouQChbUMUo5lInUuMTVZUipNeZqUFEolFIeU5rpEqWmGghoQWgLimNwfeje-_er6P4q6CsMHsjFtFwohkAIykfTkw4FUvg3BG1tsfFVLvy8oFIPIovXFILIYRPb47bG4K2uj_-Bfcz1wdwRkUNJZLxtVhX8uzTHlDPAbqlF5PQ</recordid><startdate>20120601</startdate><enddate>20120601</enddate><creator>LAN YI</creator><creator>JI, Xiao-Xia</creator><creator>HUI TAN</creator><creator>FENG, Mei-Yan</creator><creator>YI TANG</creator><creator>LING WEN</creator><creator>QI SU</creator><general>Spandidos</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20120601</creationdate><title>Involvement of Mcl1 in diallyl disulfide-induced G2/M cell cycle arrest in HL-60 cells</title><author>LAN YI ; JI, Xiao-Xia ; HUI TAN ; FENG, Mei-Yan ; YI TANG ; LING WEN ; QI SU</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c358t-1dff3a7939ff20573b4ad8a35e64bcd1754b10bc9c70518db3ad16391e09da033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Allyl Compounds - pharmacology</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>CDC2 Protein Kinase - metabolism</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Disulfides - pharmacology</topic><topic>G2 Phase Cell Cycle Checkpoints - drug effects</topic><topic>HL-60 Cells</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Myeloid Cell Leukemia Sequence 1 Protein</topic><topic>Proliferating Cell Nuclear Antigen - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2 - genetics</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering</topic><topic>Tumors</topic><toplevel>online_resources</toplevel><creatorcontrib>LAN YI</creatorcontrib><creatorcontrib>JI, Xiao-Xia</creatorcontrib><creatorcontrib>HUI TAN</creatorcontrib><creatorcontrib>FENG, Mei-Yan</creatorcontrib><creatorcontrib>YI TANG</creatorcontrib><creatorcontrib>LING WEN</creatorcontrib><creatorcontrib>QI SU</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LAN YI</au><au>JI, Xiao-Xia</au><au>HUI TAN</au><au>FENG, Mei-Yan</au><au>YI TANG</au><au>LING WEN</au><au>QI SU</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of Mcl1 in diallyl disulfide-induced G2/M cell cycle arrest in HL-60 cells</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2012-06-01</date><risdate>2012</risdate><volume>27</volume><issue>6</issue><spage>1911</spage><epage>1917</epage><pages>1911-1917</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Diallyl disulfide (DADS) has shown potential as a therapeutic agent in various cancers. Previously, we found that myeloid cell leukemia sequence 1 (Mcl1) was downregulated in DADS-induced cell cycle arrest in HL-60 human leukemia cells. Here, we investigated the role of this protein in DADS-induced G2/M cell cycle arrest in HL-60 cells. We demonstrated that DADS treatment significantly increased the proportion of G2/M phase HL-60 cells (P<0.05) and caused a time-dependent significant downregulation of Mcl1 and the cell cycle-related proteins PCNA and CDK1 (P<0.05). Small interfering RNA-mediated knockdown of Mcl1 expression in HL-60 cells arrested the cell cycle in G2/M phase. By co-immunoprecipitation, we demonstrated that Mcl1 associated with PCNA and CDK1 in G2/M cell cycle arrest in DADS-treated HL-60 cells. DADS decreased the interaction of Mcl1 with PCNA and CDK1, leading to G2/M cell cycle arrest in HL-60 cells. Mcl1 plays an important role in DADS-induced G2/M cell cycle arrest in HL-60 human leukemia cells.</abstract><cop>Athens</cop><pub>Spandidos</pub><pmid>22378300</pmid><doi>10.3892/or.2012.1704</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Allyl Compounds - pharmacology Antineoplastic Agents - pharmacology Biological and medical sciences CDC2 Protein Kinase - metabolism Cell Cycle Proteins - metabolism Cell Line, Tumor Cell Proliferation Disulfides - pharmacology G2 Phase Cell Cycle Checkpoints - drug effects HL-60 Cells Humans Medical sciences Myeloid Cell Leukemia Sequence 1 Protein Proliferating Cell Nuclear Antigen - metabolism Proto-Oncogene Proteins c-bcl-2 - genetics Proto-Oncogene Proteins c-bcl-2 - metabolism RNA Interference RNA, Small Interfering Tumors |
| title | Involvement of Mcl1 in diallyl disulfide-induced G2/M cell cycle arrest in HL-60 cells |
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